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Practice

Voriconazole-induced periostitis

Tetiana Glushko and Inés Colmegna
CMAJ October 06, 2015 187 (14) 1075; DOI: https://doi.org/10.1503/cmaj.141025
Tetiana Glushko
Division of Rheumatology, Department of Medicine, McGill University, Montréal, Que.
MD
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Inés Colmegna
Division of Rheumatology, Department of Medicine, McGill University, Montréal, Que.
MD
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A 66-year-old woman with a two-year history of T-cell prolymphocytic leukemia presented with left shoulder pain of 10 months’ duration. A month before the admission, the pain became severe, constant and disabling. She was taking voriconazole for invasive neurohistoplasmosis (300 mg twice daily for 10 months). The patient had painful restriction of the left shoulder’s active range of motion and tenderness on palpation of the chest wall and left leg. Alkaline phosphatase levels were elevated (200 [normal 25–100] U/L) and creatinine levels were normal. Smooth periosteal thickening of the left clavicle was seen on radiography (Figure 1). A bone scan showed multiple areas of increased tracer activity (Figure 2A).

Figure 1:
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Figure 1:

Radiograph of the left shoulder of a 66-year-old woman showing smooth periosteal thickening in the distal third of the clavicle (arrow).

Figure 2:
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Figure 2:

(A) Whole-body bone scan showing multiple areas of increased tracer activity involving the clavicles, ribs and long bones (arrows). (B) Follow-up bone scan showing resolution of the increased tracer activity.

The differential diagnosis included a periosteal reaction secondary to leukemia, infection-related periosteal apposition and drug-induced periostitis. After ruling out a recurrence of leukemia and infection, we diagnosed voriconazole-induced periostitis.1 Discontinuation of voriconazole led to the resolution of pain within 48 hours. At a three-month follow-up, the alkaline phosphatase level and bone scan were normal (Figure 2B). At nine months, there was no evidence of leukemic relapse or active infection.

Fluorosis (the integration of fluoride into bone structure) and promotion of bone formation by osteoblast stimulation is the proposed mechanism of voriconazole-related periostitis.2,3 Risk factors for fluorosis include renal impairment, long-term use of voriconazole at therapeutic doses, slow drug metabolism and elevated fluoride levels.2 Unlike voriconazole, other fluorinated triazoles (e.g., fluconazole and posaconazole) are not associated with periostitis.2 Drug-induced reversible periostitis has also been described in connection with prostaglandin E14 and interleukin-11.5

Footnotes

  • Competing interests: None declared.

  • This article has been peer reviewed.

  • The authors have obtained patient consent.

References

  1. ↵
    1. Wermers RA,
    2. Cooper K,
    3. Razonable RR,
    4. et al
    . Fluoride excess and periostitis in transplant patients receiving long-term voriconazole therapy. Clin Infect Dis 2011;52:604–11.
    OpenUrlCrossRefPubMed
  2. ↵
    1. Gerber B,
    2. Guggenberger R,
    3. Fasler D,
    4. et al
    . Reversible skeletal disease and high fluoride serum levels in hematologic patients receiving voriconazole. Blood 2012;120:2390–4.
    OpenUrlAbstract/FREE Full Text
  3. ↵
    1. Lindsay R
    . Fluoride and bone–quantity versus quality. N Engl J Med 1990;322:845–6.
    OpenUrlCrossRefPubMed
  4. ↵
    1. Niethammer JG,
    2. Rule KA,
    3. Lorch V,
    4. et al
    . Periosteal reaction induced by prostaglandins. Am J Perinatol 1992;9:279–80.
    OpenUrlCrossRefPubMed
  5. ↵
    1. Milman E,
    2. Berdon WE,
    3. Garvin JH,
    4. et al
    . Periostitis secondary to interleukin-11 (Oprelvekin, Neumega). Treatment for thrombocytopenia in pediatric patients. Pediatr Radiol 2003;33:450–2.
    OpenUrlCrossRefPubMed
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Canadian Medical Association Journal: 187 (14)
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Vol. 187, Issue 14
6 Oct 2015
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Voriconazole-induced periostitis
Tetiana Glushko, Inés Colmegna
CMAJ Oct 2015, 187 (14) 1075; DOI: 10.1503/cmaj.141025

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Voriconazole-induced periostitis
Tetiana Glushko, Inés Colmegna
CMAJ Oct 2015, 187 (14) 1075; DOI: 10.1503/cmaj.141025
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